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Abstract

Periodontal disease is a chronic inflammatory disease affecting the structures
supporting the teeth. It results from the interaction between a microbial biofilm on the
tooth surface and a de‐regulated host response in the periodontal tissues of a
genetically susceptible host. There are strong correlations between specific ‘red
complex’ micro‐organisms within the subgingival biofilm and disease. Dysbiosis, a
deleterious shift in the relative abundance of components of the microbiota in disease,
is a recognised property of microbiomes at other sites of the GI tract in chronic
diseases.
Exploring dysbiosis in the oral commensal microbiota using a mouse model of
periodontitis, we have shown that a ‘red complex’ organism (Porphyromonas
gingivalis) caused significantly more periodontal bone loss in specific pathogen free
(SPF) mice than controls and no bone loss in germ free (GF) mice. This confirms the oral
commensal microbiota is fundamentally required for periodontal bone loss. In
addition, low level colonisation of SPF mice with P. gingivalis led to qualitative and
quantitative changes to the microbiota; dysbiosis. The oral commensal microbiota of
the SPF mice was stable for our aging population of SPF mice and this led to increased
alveolar bone loss with age.
Through a series of co‐caging experiments we have shown that the oral commensal
microbiota of different strains of mice was transmissible into GF mice and led to
periodontal bone loss. We have also demonstrated that a dysbiotic oral commensal
microbiota was transmissible into GF mice and led to increased periodontal bone loss.
In conclusion, the oral commensal microbiota is fundamental in the pathogenesis of
periodontal disease in this mouse model. Moreover, it is dysbiosis of this oral
commensal microbiota, brought about by P. gingivalis, that drives accelerated alveolar
bone loss. We propose that P. gingivalis be considered as a keystone species